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Nervous system

About: Nervous system is a research topic. Over the lifetime, 16729 publications have been published within this topic receiving 847181 citations.


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Journal ArticleDOI
TL;DR: Observed alterations provide evidence for extensive plastic reorganization in the adult human cortex following nervous system injury, but they are not a sufficient cause of the phantom phenomenon termed 'facial remapping'.
Abstract: MAGNETIC source imaging revealed that the topographic representation in the somatosensory cortex of the face area in upper extremity amputees was shifted an average of 1.5 cm toward the area that would normally receive input from the now absent nerves supplying the hand and fingers. Observed alterat

355 citations

Journal ArticleDOI
TL;DR: The goal of this review is to present evidence for signaling cascades in these cell types that not only will deepen the understanding of the genesis of neuropathic pain but also may help to identify new targets for pharmacological intervention.
Abstract: Damage to the nervous system can cause neuropathic pain, which is in general poorly treated and involves mechanisms that are incompletely known. Currently available animal models for neuropathic pain mainly involve partial injury of peripheral nerves. Multiple inflammatory mediators released from damaged tissue not only acutely excite primary sensory neurons in the peripheral nervous system, producing ectopic discharge, but also lead to a sustained increase in their excitability. Hyperexcitability also develops in the central nervous system (for instance, in dorsal horn neurons), and both peripheral and spinal elements contribute to neuropathic pain, so that spontaneous pain may occur or normally innocuous stimuli may produce pain. Inflammatory mediators and aberrant neuronal activity activate several signaling pathways [including protein kinases A and C, calcium/calmodulin-dependent protein kinase, and mitogen-activated protein kinases (MAPKs)] in primary sensory and dorsal horn neurons that mediate the induction and maintenance of neuropathic pain through both posttranslational and transcriptional mechanisms. In particular, peripheral nerve lesions result in activation of MAPKs (p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase) in microglia or astrocytes in the spinal cord, or both, leading to the production of inflammatory mediators that sensitize dorsal horn neurons. Activity of dorsal horn neurons, in turn, enhances activation of spinal glia. This neuron-glia interaction involves positive feedback mechanisms and is likely to enhance and prolong neuropathic pain even in the absence of ongoing peripheral external stimulation or injury. The goal of this review is to present evidence for signaling cascades in these cell types that not only will deepen our understanding of the genesis of neuropathic pain but also may help to identify new targets for pharmacological intervention.

354 citations

Journal ArticleDOI
28 Jan 1994-Science
TL;DR: The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger, which provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.
Abstract: The long-lasting increase in synaptic strength known as long-term potentiation has been advanced as a potential physiological mechanism for many forms of both developmental and adult neuronal plasticity. In many models of plasticity, intercellular communication has been proposed to account for observations in which simultaneously active neurons are strengthened together. The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger. This distributed potentiation provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.

352 citations

Journal ArticleDOI
10 Nov 1988-Nature
TL;DR: Quantitative studies of a simple part of the nervous system in mammals provide evidence that neuronal geometry and innervation are regulated by long-term trophic interactions between neurons and their targets.
Abstract: A remarkable feature of nerve cells is the complex and variable pattern of their axonal and dendritic branches. Quantitative studies of a simple part of the nervous system in mammals provide evidence that neuronal geometry and innervation are regulated by long-term trophic interactions between neurons and their targets. This trophic linkage may explain how nerve cells adjust their function to the needs of bodies that vary markedly in size and form.

352 citations

Journal ArticleDOI
TL;DR: Gene expression in neurons persists for a long time, even at postnatal stages, after electroporation, which could be used to analyze roles of genes not only in embryonic development but also in higher order function of the nervous system, such as learning.
Abstract: This protocol describes a basic method for in vivo electroporation in the nervous system of embryonic mice. Delivery of electric pulses following microinjection of DNA into the brain ventricle or the spinal cord central canal enables efficient transfection of genes into the nervous system. Transfection is facilitated by forceps-type electrodes, which hold the uterus and/or the yolk sac containing the embryo. More than ten embryos in a single pregnant mouse can be operated on within 30 min. More than 90% of operated embryos survive and more than 90% of these survivors express the transfected genes appropriately. Gene expression in neurons persists for a long time, even at postnatal stages, after electroporation. Thus, this method could be used to analyze roles of genes not only in embryonic development but also in higher order function of the nervous system, such as learning.

351 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023247
2022510
2021371
2020409
2019375
2018357